Left ventricular biplane cineangiography, micromanometry, and endomyocardial biopsies were performed in 27 patients with aortic stenosis (AS) and in 17 patients with aortic insufficiency (AI). Twenty-three patients with AS and 15 with AI were restudied at an intermediate time (18 months after successful valve replacement), and nine patients with AS and six with AI were restudied late (70 and 62 months after surgery). Biopsy samples were evaluated for muscle fiber diameter, percent interstitial fibrosis, and volume fraction of myofibrils. In control biopsy samples obtained from five donor hearts at transplantation, these morphometric variables averaged 21.2 ,jm, 7.0%, and 57.2%, respectively. After surgery, mass determined by cineangiography decreased from 186 to 115 and 94 g/m2 in patients with AS and from 201 to 131 and 93 g/m2 in patients with AI. At the three studies, muscle fiber diameter was 30.9, 28.0, and 28.7 ,um in patients with AS and was 31.4, 27.6, and 26.4 ,um in patients with AI. Percent interstitial fibrosis was 18.2, 25.8, and 13.7% in patients with AS and was 20.4, 23.7, and 19.2% in patients with AI. Left ventricular fibrous content decreased from 34.2 to 29.8 and to 12.7 g/m2 in patients with AS and from 42.1 to 28.9 and to 18.9 g/m2 in patients with AI. Volume fraction of myofibrils was 57.7, 56.8, and 49.0% in patients with AS and was 56.8, 56.6 and 48.8% in patients with AI. Thus, the decrease of muscle mass determined by cineangiography at the intermediate time after valve replacement is mediated by regression of myocardial cellular hypertrophy in patients with AS and AI and in addition by a decrease of fibrous content in patients with AI. Late after surgery, left ventricular fibrous content also decreases in patients with AS. This late decrease associated with minor changes of end-diastolic volume may be important for improvement of increased diastolic myocardial stilfness. Even 6-7 years after valve replacement, incomplete regression of structural abnormalities of left ventricular hypertrophy still exists compared with the normal myocardium. The residually increased relative interstitial fibrosis and the small late postoperative decrease of volume fraction of myofibrils, associated with a prosthesis-related slight left ventricular pressure increase, are at the origin of a persistent systolic overload at the myofibrillar level. (Circulation 1989;79:744-755) Ch hronic pressure or volume overload or both in aortic valve disease is associated with marked left ventricular hypertrophy, evidenced by angiographyl-9 and microscopy.10-14This process of secondary hypertrophy is accompanied invariably by an increase in interstitial connective tissue.10-2,15,16 Correction of the abnormal hemody-

There is a high in-hospital mortality rate when CS develops as a result of VSR. Ventricular septal rupture may occur early after infarction, and women and the elderly may be more susceptible. Although the prognosis is poor, surgery remains the best therapeutic option in this setting.

To assess the time course and extent of regression of myocardial hypertrophy after removal of the inciting hemodynamic stress, 21 patients with either aortic stenosis or aortic insufficiency were studied preoperatively, after an intermediate period (1.6 + 0.5 years), and late (8.1 + 2.9 years) after aortic valve replacement, and results were compared with those in 11 control patients. After aortic valve replacement there was significant hemodynamic improvement, with a fall in the left ventricular end-diastolic volume index (164 + 73 to 105 + 35 ml/m2, p < .01), a fall in left heart filling pressure (19 + 9 to 12 + 5 mm Hg, p < .01), and maintenance of the cardiac index (3.3 + 0.8 to 3.5 ± 0.8 liters/min/m2, NS) and left ventricular ejection fraction (60 ± 13% to 64 ± 10%, NS). By the late study the cardiac index (4.0 ± 0.6 liters/min/m2, p < .01) and left ventricular ejection fraction (66 ± 15%, p < .05) had further increased and were significantly greater than before surgery. For the group as a whole, the left ventricular muscle mass index fell 31% after surgery by the time of the intermediate postoperative study (174 ± 38 vs 120 ± 29 g/m2, p < .01), and a further 13% from the intermediate to the late study (105 ± 32 g/m2, p < .05). At the preoperative study left ventricular muscle mass index was greatest in those patients with aortic insufficiency (191 ± 36 g/m2), and greater in those with aortic stenosis (158 ± 33 g/m2) than in control subjects (85 ± 9 g/m2, p < .05). At the intermediate postoperative study left ventricular muscle mass index remained significantly higher in both those with preoperative aortic insufficiency (128 ± 29 g/m2) and those with stenosis (114 ± 27 g/m2) than in the control subjects (p < .01). By the time of the late postoperative study there were no longer any significant differences in left ventricular muscle mass index. Thus, the regression of myocardial hypertrophy is a process that occurs over many years after correction of the primary hemodynamic abnormality. As this process of myocardial remodeling occurs, continued improvement in cardiac function may occur, and the improvement occurring between the intermediate and late postoperative studies at a slight but constant afterload excess (inherent in the relative stenosis of the aortic prosthesis) suggests that the hypertrophied myocardium is operating at a reduced level compared with normal myocardium. Circulation 77, No. 6, 1345No. 6, -1355No. 6, , 1988 LEFT VENTRICULAR pressure and volume overloads in response to aortic valve stenosis and aortic valve insufficiency lead to a marked hypertrophic response of the myocardium, likely as an adaptative response to normalize the increased wall stress accompanying these states.' While this allows for maintenance

During primary PCI, physician experience significantly modifies the hospital volume-outcome relationship. Therefore, policymakers need to consider physician experience when developing strategies to improve access to primary PCI.